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420 Non-neoplastic Lesions of the Placenta, Pathology of the Placenta
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Non-neoplastic Lesions of the Vulva 423
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Cicatricial pemphigoid is a bullous disorder
Non-neoplastic Lesions
of the Vulva (Inflammations,
Dermatologic Conditions,
Infections), Pathology
of the Vulva
Jennifer Crimmins1, Aleodor Andea2and
Maria Angelica Selim
1
Department of Pathology, Duke University
Medical Center, Durham, NC, USA
2
Department of Pathology, University of
Michigan, Ann Arbor, MI, USA
Bullous Pemphigoid and Cicatricial
Pemphigoid
Synonyms
Cicatricial pemphigoid; Mucous membrane
pemphigoid.
Definition
Bullous and cicatricial pemphigoid are subepidermal autoimmune bullous disorders that may
involve the vulva. Cicatricial pemphigoid more
commonly involves the vulva than bullous
pemphigoid. Both disorders may demonstrate
serum autoantibodies to 230-kDa BPAg1 and
180-kDa BPAg2 identified by immunoblotting
(Hoang et al. 2014). Other target antigens in cicatricial pemphigoid include laminin 5, laminin 6,
type VII collagen, and integrin β
et al. 2002).
Clinical Features
Bullous pemphigoid is a chronic bullous eruption
that classically affects middle-aged toelderly individuals in the sixth to eighth decade; however,
children can also be affected. Common sites of
involvement include trunk, groin, axillae, and
flexural areas. The vulva may be involved in 9%
of adult patients and 40% of children with generalized bullous pemph igoid (Farrell et al. 1999).
A localized variant of bullous pemphigoid involving only the vulva can also be seen and may affect
both children and adults.
1
subunit (Chan
4
with a predilection for mucosal sites that heals
with scarring. The conjunctiva and oral mucosa
are most common mucosal sites affected. The
vulva can be affected alone or in combination
with other mucosal sites. In adults with cicatricial
pemphigoid, approximately 50% have vulval
involvement (Marren et al. 1993). Cicatricial
pemphigoid of the vulva can raise false concern
for sexual abuse when occurring in children
(Hoque et al. 2006; Levine et al. 1992).
• Age
Bullous pemphigoid most commonly affects
elderly patients in the sixth to eighth decade;
however, can also rarely affect children and has
been described localized to the vulva (Fisler
et al. 2003; Nemeth et al. 1991; Saad et al.
1992; Kirtschig et al. 1994; DeCastro et al.
1985, Nagano et al. 1994). Localized bullous
pemphigoid has been reported in children ages
7–12 (Fisler et al. 2003). Similarly, cicatricial
pemphigoid most commonly affects middle-
aged to older patients; however, children are
also affected.
• Site
Bullous pemphigoid can affect the vulva alone
or as extension from the groin. The vagina is
very rarely affected (Wan-Peng Lim and
Bystryn 1978). Cicatricial pemphigoid affects
the vulva with or without vaginal involvement.
Extension to the perianal area can also be seen.
• Treatment
Mild cases may resolve with potent topical
steroids; however, systemic therapy with cor-
ticosteroids is a mainstay of treatment. Other
successful reported therapies in bullous
pemphigoid include dapsone, sulfones, cyclo-
sporine, chlorambucil, and azathioprine (Fisler
et al. 2003). In cicatricial pemphigoid, other
successful therapies include sulfapyridine,
minocycline, mycophenolate mofetil, and
intravenous immunoglobulin (IVIg) (Garg
and Mittal 2012). Intralesional steroids have
been used in cicatricial pemphigoid to mini-
mize scarring (Wan-Peng Lim and Bystryn
1978). In patients with cicatricial pemphigoid,
N
424 Non-neoplastic Lesions of the Vulva
https://t.me/med1917
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 1 Tense blisters of bullous
pemphigoid with erosions from ruptured bullae.
(Courtesy of Dr. Libby Edwards)
patients should undergo evaluation for ocular
involvement.
• Outcome
Scarring in cicatricial pemphigoid can lead to
labial fusion and introital shrinkage, which
may cause urinary and sexual dysfunction
(Chan et al. 2002).
Macroscopy
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 2 Nonspecific erosions and severe
scarring with loss of architecture typical of cicatricial
pemphigoid; only the coalescing round erosions on the
right anterior modified mucous membrane hint at the
underlying blistering morphology. (Courtesy of Dr. Libby
Edwards)
Bullous Pemphigoid
On physical exam, bullous pemphigoid typically
presents with tense blisters on an erythematous
base (Fig. 1). Lesions may begin as urticarial.
Nikolsky sign is negative (Hoang et al. 2014).
Cicatricial Pemphigoid
The exam findings in cicatricial pemphigoid are
similar to bullous pemphigoid; however, they may
also present with nonspecific erosions with few or
no intact blisters. Lesions are associated with
scarring and may lead to labial fusion and introital
shrinkage (Garg and Mittal 2012; Hoque et al.
2006) (Fig. 2). Nikolsky sign is positive (Hoang
et al. 2014).
Microscopy
Histopathologically, bullous and cicatricial
pemphigoid are similar. Both demonstrate a
subepidermal vesicle with variable numbers of
eosinophils within bullae and dermis (Fig. 3a, b).
Neutrophils may or may not be present, most
frequently seen in early phase. In cicatricial
pemphigoid, subepidermal scarring is seen
(Fig. 4a–c) (Hoang et al. 2014).
On direct immunofluorescence, linear IgG and
C3 deposition is seen at the basement membrane
zone. IgA and/or IgM deposition may also be
seen. Indirect immunofluorescence on salt split
skin usually demonstrates serum autoantibodies
on the roof of the blister.
Differential Diagnosis
Cicatricial pemphigoid can clinically be misdiagnosed as lichen sclerosus due to the presence
of scarring with labial fusion and occasional
perianal involvement. The presence of sclerosis
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Non-neoplastic Lesions of the Vulva (Inflammations,
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of the Vulva, Fig. 3 Histologically, bullous pemphigoid
is characterized by a subepidermal bullae containing
eosinophils (a); these cells are also seen lining the
dermal-epidermal junction at the edge of the bullae (b)
and in a perivascular distribution
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Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 4 Histologically, cicatricial
pemphigoid displays a subepidermal blister (a) with presence of fibrosis in the upper dermis (b) and eosinophils in a
perivascular and interstitial pattern (c)
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in the histology and negative direct immunofluorescence results point toward lichen sclerosus
and should resolve this differential diagnostic
consideration (Marren et al. 1996). Epidermal
bullosa acquisita also shows a s ubepidermal bullae, usually pauci-inflammatory. They differentiate as the target in this disease is type VII
collagen, and in salt-split skin test t he base of
the vesicle is stained. Linear IgA disease, bullous
disorder associated with inflammatory bowel
disease, in particularly ulcerative colitis, presents
with a subepidermal bullae. Immunofluorescence test will identify this entity by the presence
of linear IgA deposition along the dermalepidermal junction. As previously mentioned,
cicatricial pemphigoid can falsely raise concern
for sexual abuse in children on clinical exam.
Immunofluorescent test is a useful test in this
diagnostic dilemma.
Vulvovaginal Candidiasis
Synonyms
Candidal vulvovaginitis.
Definition
Infection of the genitalia with Candida species,
more commonly caused by Candida albicans.
Clinical Features
• Incidence
Candida infections are common, and
vulvovaginal candidiasis is the most common
form of mucosal candidiasis. About 70–75% of
women experience at least one episode during
their life, and half will have multiple episodes.
In addition, 15–30% of women are asymptomatic carriers (Goncalves et al. 2016).
• Age
Vulvovaginal candidiasis tends to affect
women of reproductive age, less common
before menarche and after menopause (Sobel
et al. 1998).
• Site
Intertriginous areas.
• Treatment
Treatment includes antifungal therapy with
topical or oral agents such as polyens (e.g.,
nystatin) or azoles (e.g., fluconazole or
itraconazole) (Goncalves et al. 2016).
• Outcome
Topical or oral treatments achieve a cure rate
of 75–90% depending on the age nt used
(Goncalves et al. 2016). Most infections are
superficial and uncomplicated. However,
when left untreated, vulvovaginal candidia-
sis can lead to complications including pelvic
inflammatory di sease, infertility, ectopic
pregnancy, spontaneous abortion, and men-
strual disorders (Goncalves et al. 2016).
Macroscopy
An acute and a chronic form have been
described. Acute superficial candidiasis presents with a “beefy-red,” moist appearance
with vulvar erythema, edema, fissures, and a
nonmalodorous white vaginal discharge
(Goncalves et al. 2016). Chronic infection can
occur in immunodeficiencies, endocrinopathies,
or nutritional deficiencies and appears as
lichenified plaques with erythema and minimal
discharge.
Microscopy
Acute superficial candidiasis is characterized on
histology by epidermal acanthosis and spongiosis
with spongiform or subcorneal pustules and exocytosis of neutrophils (Fig. 5). In contrast, chronic
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 5 The lesion shows acanthosis, epi-
dermal spongiosis, and a mild superficial perivascular lymphocytic infiltrate. Arrow indicates fungal pseudohyphae
with vertical orientation in stratum corneum
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Definition
Sexually transmitted, benign proliferative squamous lesion with warty exophytic morphology
or flat (nonwarty), caused by human papillomavirus (HPV) infection.
Clinical Features
• Incidence
HPV infection and condyloma acuminatum are
very common. About 20–40% of sexually
active women are infected with HPV with 5.5
million new HPV infections per year in the
USA for a total prevalence of 20 million. The
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 6 GMS special stain reveals yeasts
and pseudohyphae within stratum corneum with perpendicular orientation to the epidermis
incidence of genital condylomas has increased
among women from 0.013% in 1950 to 1%
currently (Gall 2001).
• Age
Condyloma acuminatum has a predilection for
mucocandidiasis demonstrates epidermal
acanthosis and scale crust. Stains for fungal
organisms including PAS with diastase or GMS
reveal budding yeasts and pseudohyphae in stratum corneum often oriented perpendicular to the
epidermis (Fig. 6).
young, sexually active women in the second to
third decade of life (Gall 2001).
• Site
Typically involves labia minora, introitus, and
the medial aspect of labia majora.
• Treatment
Various methods are used to remove condylo-
Differential Diagnosis
The histology of candidiasis may overlap with
that of eczematous dermatitis, lichen simplex
chronicus, intertrigo, and psoriasis, and in this
context special stains for fungi should be
employed to rule out a fungal infection.
Dermatophytosis can also affect the genital
area; however, it tends to involve the skin of the
groin rather than vulvar mucosa and the rash
tends to be annular. Special stains for fungi will
reveal hyphae in stratum corneum; however, at
times it is not possible to differentiate dermatophytes from Candida and correlation with clinical presentation andmicrobiology culture studies
mas including surgical excision, laser ablation,
cryotherapy, and topical application of
imiquimod, 5-fluorouracil, or podophyllin
(O’Mahony 2005).
• Outcome
Condylomas are benign; however, patients
may suffer from multiple recurrences. Some
lesions will regress without intervention; how-
ever, the viral infection may persist and factors
that produce immunosuppression may lead to
recurrences. Some condylomas are associated
with high-risk HPV, and this may account for
progression of some lesions to high-grade
squamous intraepithelial lesions (HGSIL).
is required for a precise diagnosis (Day
et al. 2016).
Macroscopy
Usually, multiple lesions are present involving
moist areas of the vulva. Two major types can be
Condyloma Acuminatum
encountered: exophytic condyloma (condyloma
acuminatum) and flat condyloma. The exophytic
Synonyms
Low-grade squamous intraepithelial lesion
(LGSIL); Vulvar intraepithelial neoplasia I
(VIN I).
type presents as “cauliflower-like” masses with
velvety, fleshy appearance (Fig. 7). The flat condylomas appear as white, erythematous, or hyperpigmented papules or macules.
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Non-neoplastic Lesions of the Vulva (Inflammations,
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of the Vulva, Fig. 8 Low magnification shows a papillary
architecture with acanthosis, bulbous rete, and an undulating
interface with the dermis or submucosa
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 7 Condylomas presenting as multiple
“cauliflower-like” lesions with an exophytic appearance
Microscopy
Exophytic condylomas demonstrate a papillary
architecture at low magnification with bulbous rete
and an undulating interface with the dermis or submucosa (Fig. 8). The lesion shows hyperkeratosis
and parakeratosis with accentuation of the granular
layer. Foci of keratinocytes with enlarged and irregular nuclei and perinuclear clear halos representing
HPV cytopathic changes or koilocytosis are seen in
the superficial epithelial layers (Fig. 9). Flat condy-
lomas lack the papillary architecture but demonstrate acanthosis and hyperkeratosis; they are less
common in the vulva compared to cervix (Medeiros
et al. 2005;Yangetal.2017).
Immunophenotype
Immunohistochemistry for p16 shows typically
patchy staining in exophytic condylomas which
helps to differentiate from HGSIL (Walts et al.
2006). It can be diffuse with “block pattern” in
condylomas associated with HR-HPV infection
limiting the utility of p16 in this context in
differentiating LSIL from HSIL (Lewis
et al. 2017).
Non-neoplastic Lesions of the Vulva (Inflammations,
Dermatologic Conditions, Infections), Pathology
of the Vulva, Fig. 9 At high magnification, condylomas
show hyperkeratosis and parakeratosis with foci of
koilocytosis
Molecular Features
Exophytic condylomas are caused by infection
with low-risk HPV, and most commonly serotypes 6 and 11 (Gall 2001; Logani et al. 2003).
Flat condylomas can be caused by low-risk and
also high-risk HPV (Logani et al. 2003; Srodon
et al. 2006).
Differential Diagnosis
Fibroepithelial stromal polyps can be papillomatous; however, they lack epithelial acanthosis and
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koilocytosis. Seborrheic keratosis (SK) demonstrates a basaloid morphology and keratin pseudocysts. However, consi dering that HPV can be
demonstrated in cases of vulvar SK, some consider these lesions to represent a variant of condyloma (Bai et al. 2003; Medeiros et al. 2005).
HGSIL and squamous cell carcinoma demonstrate nuclear atypia and mitotic figures involving
the entire thickness of the epidermis. Verrucous
carcinoma is a rare form of vulvar squamous cell
carcinoma that may resemble condyloma especially in small biopsies. As opposed to condyloma, verrucous carcinoma demonstrates an
endophytic pushing growth in the stroma and
lacks koilocytosis (Yang et al. 2017). Finally,
condyloma lata represents a type of secondary
syphilis involving the vulva, characterized by a
verrucous morphology that resembles condyloma
acuminatum. As opposed to condyloma
acuminatum, condyloma lata demonstrates an
inflammatory infiltrate with plasma cells, and
endothelial swelling, and does not show
koilocytosis. In addition, spirochetes can be identified with Steiner or spirochete immunohistochemical stains.
Eczematous Dermatitis
Synonyms
Spongiotic dermatitis.
Definition
Eczematous dermatitis is a common inflammatory
condition affecting the vulva that encompasses
atopic dermatitis and contact dermatitis, both irritant and allergic. These dermatitides are all characterized by spongiosis, or intercellular
intraepidermal edema, histologically. In the
vulva, contact dermatitis is more common than
atopic dermatitis. Among exogenous causes of
eczematous dermatitis, irritant contact dermatitis
is more common than allergic contact dermatitis
(Hoang et al. 2014;O’Gorman and Torgerson
2013; Moyal-Barracco and Wendling 2014). Clin-
ically, patients may present with pruritus, dryness,
burning, and sometimes pain and dyspareunia
(Hoang et al. 2014).
Irritant contact dermatitis is caused by local
toxic effect of an offending agent and typically
evolves within minutes to hours of exposure. Vulvar skin is particularly susceptible to irritants due
to the increased moisture, heat, occlusion, and
friction present at this site. Urinary incontinence
is one of the main causes of irritant dermatitis
(Moyal-Barracco and Wendling 2014). Other
commonly implicated irritants include garments,
hygiene sprays, soap, condoms, spermicides, vaginal douches, and menstrual and incontinence
pads, among others (Bauer et al. 2005). Abortifacients have been historically implicated as a cause
of irritant contact dermatitis (Shull 1941;
Vandergriff and Diddle 1966).
Allergic contact dermatitis is a delayed type
(type IV) hypersensitivity reaction to an external
agent and as such clinical symptoms develop
24–48 hours after exposur e. There are numerous
implicated allergens including local anesthetics,
topical antibiotics, topical corticosteroids, herbal
extracts (as in sitz baths or cosmetic preparations),
preservatives in cosmetics and toiletries, perfumes, and latex (Bauer et al. 2000;O’Gorman
and Torgerson 2013).
Atopic dermatitis is the result of the interaction
of both genetic and environmental factors and is
part of the atopic triad, which also includes allergic rhinitis and asthma. A personal or family
history of atopy is often identified in individuals
with atopic dermatitis. Additionally, patients with
atopic dermatitis are prone to developing allergic
contact dermatitis.
Clinical Features
The clinical presentation varies somewhat
depending on chronicity. In acute eczematous
dermatitis, vulvar erythema, edema, and vesicles
can be seen (Fig. 10). Subacute to chronic stages
are characterized by erythematous to lichenified
and excoriated patches and plaques often with
scaling and accentuated skin markings (Fig. 11)
(Hoang et al. 2014; Bauer et al. 2005; Elsner et al.
1990; Pichardo-Geisinger 2017). Contact derma-
titis tends to display more well-demarcated
plaques than are seen in atopic dermatitis, which
corresponds to the area of exposure. Postinflammatory pigmentary alteration, either
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